These studies propose to investigate further the mechanism of glomerular immune deposit formation in membranous nephropathy using the autologous immune complex nephropathy (AICN) and passive Heymann nephritis (PHN) models in rats. They will attempt to determine if the mechanism of deposit formation in AICN is similar to the in situ mechanism already established in PHN by comparing rat antibody eluted from AICN kidneys with heterologous anti-FX1A IgG with respect to the kinetics of glomerular antibody binding in vitro and in vivo, deposit formation in the isolated perfused rat kidney and competitive binding assays. Studies will also be carried out to assess the role of antibody charge and antibody size in regulating the rate of subepithelial immune deposit formation in vivo. The increase in glomerular permeability induced immediately by injection of F(ab)2 and Fab' prime fragments of heterologous anti-Fx1A IgG will be characterized with respect to kinetics of deposit formation and mechanisms of glomerular injury involved. Further studies will be done to document the role of the terminal complement components in mediating the complement-dependent, neutrophil indepent proteinuria defined in the PHN model. It is hoped that these studies will further clarify the mechanisms of subepithelial immune deposit formation and how such deposits mediate immune glomerular injury.